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Cardiovascular Research 1998 38(1):206-214; doi:10.1016/S0008-6363(97)00319-2
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

The enhanced pressor response in type 2 diabetes is not based upon a generalized increase in vascular responsiveness

F.C Huvers*, P.W de Leeuw, C.H.A de Haan, A.J.H.M Houben, C Buijs and N.C Schaper

Dept. of Internal Medicine, Div. of Endocrinology and General Internal Medicine, Cardiovascular Research Institute Maastricht, University Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, Netherlands

* Corresponding author. Tel.: +31 (43) 3877011; fax: +31 (43) 3875006; e-mail: F.Huvers@aig.azn.nl

Objective: The present study was performed to discriminate between central and peripheral effects of noradrenaline (NA) in normotensive, non-obese, type 2 diabetic patients. Methods: Study I: In 10 patients and 10 healthy volunteers (HV) cumulative doses of NA were infused intravenously until mean arterial pressure (MAP) rose with 20 mmHg, and subsequently the effects on the forearm blood flow (FBF) was measured. Also, the FBF response to intra-arterial NA (0.025, 0.1, 0.4 µg min–1) was measured. Study II: In 13 patients and 14 HV the venous constrictor response to a cumulative local infusion of NA in a dorsal hand vein was determined. Results: In study I the circulating plasma NA concentrations inducing a rise in MAP of 20 mmHg, were lower in the type 2 patients relative to the HV (p<0.01). The relationship between changes in pressure and changes in heart rate were similar in both groups. Moreover, FBF responsiveness to intra-arterial NA was not different between the two groups. The slopes of the deltaMAP/NA regression lines were correlated with basal insulin levels and relative insulin resistance in the healthy volunteers (R=0.77, p<0.01, and R=0.83, p<0.01), but not in the type 2 diabetic patients. In study II no differences were observed in the dose generating half maximum (ED50) and the maximum (Emax) response to NA between the type 2 patients and the HV. Conclusions: Non-obese normotensive type 2 patients have an increased pressor response to NA, which is not based upon a defect in skeletal muscle resistance arterioles, peripheral veins, or a defect in the baroreceptor system. Therefore, in type 2 diabetes the noradrenergic responsiveness of other vascular beds, such as the splanchnic or renal, must be enhanced.

KEYWORDS Noradrenaline; Blood pressure; Insulin; Type 2 diabetes; Forearm; Hand vein


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